TREM-1 factor:
Triggering receptors expressed on myeloid cells-1 is a key inflammatory amplifier that interacts with a number of TLR pathways depending on the severity of the inflammatory condition (He, Yang, Wang, Jia, Xie & Zhou, 2019; Youssef et al., 2009). According to Sun et al’s research, TREM-1 was first revealed to be produced in the context of SAH and has been linked to the pathogenesis of BBB disruption. This is one of EBI’s most serious pathological symptoms (Sun, Duan, Jing, Wang, Hou & Zhang, 2019; Sun, Ma, Jing, Wang, Hao & Wang, 2017a; Sun, Ma, Jing, Wang, Hao & Wang, 2017b). According to a new research, TREM-1 is necessary for SYK mobilization and downstream activation of CARD9/NF-κB and NLRP3/caspase-1 in microglia following stroke (Xu et al., 2019a) . TREM-1 inhibition by LP17 significantly reduced the severity of EBI, and the protective effects were attributed to reduction of downstream p38MAPK/MMP-9 activation and hence ZO-1 preservation (Sun, Duan, Jing, Wang, Hou & Zhang, 2019). TREM-1 activation can be inhibited by fusion proteins or synthetic inhibitory peptides, which can reduce the production of pro-inflammatory mediators and leukocyte recruitment (Boufenzer et al., 2015; Schenk, Bouchon, Seibold & Mueller, 2007). Neuroinflammation has been linked to post-stroke impairment in the past (Yirmiya & Goshen, 2011). According to the findings of (Xu et al., 2019a) , inhibiting TREM-1 improves long-term neurobehavioral deficits in the hippocampus following ischemic stroke by boosting cell proliferation and synaptic plasticity. According to the evidence described above, TREM-1 may have a role in the inflammatory pathways that contribute to EBI after SAH.